ArticleMolecular biology of the cell2015
Heterochromatin formation via recruitment of DNA repair proteins.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Evidence of centromeric histone 3 chaperone involved in DNA damage repair pathway in budding yeast.eLife · 2025Article
- Article
- A Role for the Mre11-Rad50-Xrs2 Complex in Gene Expression and Chromosome Organization.Molecular cell · 2021Article
- tRNA Genes Affect Chromosome Structure and Function via Local Effects.Molecular and cellular biology · 2019Article
- Smc5/6 Is a Telomere-Associated Complex that Regulates Sir4 Binding and TPE.PLoS genetics · 2016Article
- Linking replication stress with heterochromatin formation.Chromosoma · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Heterochromatin formation and nuclear organization are important in gene regulation and genome fidelity. Proteins involved in gene silencing localize to sites of damage and some DNA repair proteins localize to heterochromatin, but the biological importance of these correlations remains unclear. In this study, we examined the role of double-strand-break repair proteins in gene silencing and nuclear organization. We find that the ATM kinase Tel1 and the proteins Mre11 and Esc2 can silence a reporter gene dependent on the Sir, as well as on other repair proteins. Furthermore, these proteins aid in the localization of silenced domains to specific compartments in the nucleus. We identify two distinct mechanisms for repair protein-mediated silencing-via direct and indirect interactions with Sir proteins, as well as by tethering loci to the nuclear periphery. This study reveals previously unknown interactions between repair proteins and silencing proteins and suggests insights into the mechanism underlying genome integrity.
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Registered trials
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